Analyses of lncRNA and mRNA profiles in recurrent atrial fibrillation after catheter ablation.

Background: Atrial fibrillation (AF) is the most common cardiac arrhythmia worldwide. Catheter ablation has become a crucial treatment for AF. However, there is a possibility of atrial fibrillation recurrence after catheter ablation.

Association between systemic inflammatory response index and left ventricular remodeling and systolic dysfunction in atrial fibrillation patients.

Background: Cardiac remodeling and dysfunction can be caused by atrial fibrillation (AF). The aim of this research is to investigate the relationship between the systemic inflammatory response index (SIRI) and left ventricular (LV) remodeling and systolic function in individuals with AF.

Methods: 416 patients with AF who were admitted to the Second Department of Cardiology in the East Ward of the Qingdao Municipal Hospital between January 2020 and May 2022 were included in the present retrospective research.

Loss of α7nAChR enhances endothelial-to-mesenchymal transition after myocardial infarction via NF-κB activation.

The myocardial fibrosis in response to myocardial infarction (MI) is closely related to the dysbalance of endothelial-to-mesenchymal transition (EndMT). Although numerous reports indicate that α7 nicotinic acetylcholine receptor (α7nAChR) activates the cholinergic anti-inflammatory pathway (CAP) to regulate the magnitude of inflammatory responses, the role of α7nAChR in myocardial fibrosis, as well as the underlying mechanisms, have not been elucidated. In this study, we evaluated cardiac function, fibrosis, and EndMT signaling using a mouse model of MI and interleukin (IL)-1β-induced human cardiac microvascular endothelial cells (HCMECs).

LncRNA LINC00961 regulates endothelial‑mesenchymal transition via the PTEN‑PI3K‑AKT pathway.

The long noncoding RNA LINC00961 plays a crucial role in cancer and cardiovascular diseases. In the present study, the role and underlying mechanism of LINC00961 in endothelial‑mesenchymal transition (EndMT) induced by transforming growth factor beta (TGF‑β), was investigated. Human cardiac microvascular endothelial cells were transfected with LV‑LINC00961 or short hairpin LINC00961 plasmids to overexpress or knock down LINC00961 in the cells, respectively.

Relationship between Plasma Trimethylamine N-Oxide Levels and Renal Dysfunction in Patients with Hypertension.

Introduction: Trimethylamine N-oxide (TMAO) is a metabolite produced by gut bacteria. Although increased TMAO levels have been linked to hypertension (HTN) and chronic kidney disease (CKD) with poor prognosis, no clinical studies have directly addressed the relationship between them. In this study, we investigated the relationship between TMAO and renal dysfunction in hypertensive patients.

Metformin Attenuates Hypoxia-induced Endothelial Cell Injury by Activating the AMP-Activated Protein Kinase Pathway.

Metformin reduces the incidence of cardiovascular diseases, and potential underlying mechanisms of action have been suggested. Here, we investigated the role of metformin in endothelial cell injury and endothelial-mesenchymal transition (EndMT) induced by hypoxia. All experiments were performed in human cardiac microvascular endothelial cells (HCMECs).

Protective effects of acetylcholine on hypoxia-induced endothelial-to-mesenchymal transition in human cardiac microvascular endothelial cells.

Endothelial-to-mesenchymal transition (EndMT) has been reported as a key factor in myocardial fibrosis. Acetylcholine (ACh), a neurotransmitter of the vagus nerve, has been confirmed to exert cardio-protective properties with unclear mechanisms. In this study, the specific markers of cell injury, EndMT, inflammation, and autophagy were measured.

Klotho improves diabetic cardiomyopathy by suppressing the NLRP3 inflammasome pathway.

Aims: NLRP3 inflammasome activation is essential for the development and prognosis of diabetic cardiomyopathy (DCM). The anti-aging protein Klotho is suggested to modulate tissue inflammatory responses. The aim of the present study was to examine the protective effects of Klotho on DCM.

Vaspin prevents myocardial injury in rats model of diabetic cardiomyopathy by enhancing autophagy and inhibiting inflammation.

NLRP3 inflammasome activation plays an important role in diabetic cardiomyopathy (DCM). It is known that autophagy is related to the activation of inflammasomes during oxidative stress. Visceral adipose tissue-derived serine protease inhibitor (Vaspin), is an adipocytokine that has been shown to exert a protective effect on autophagic activity, but whether and how Vaspin improves myocardial damage in DCM remain unclear.

Vaspin Prevents Tumor Necrosis Factor-α-Induced Apoptosis in Cardiomyocytes by Promoting Autophagy.

Visceral adipose tissue-derived serine protease inhibitor (Vaspin) is an adipocytokine that has been shown to exert anti-inflammatory effects and inhibits apoptosis under diabetic conditions. This study was designed to investigate the impact of vaspin on autophagy in tumor necrosis factor (TNF)-α-induced injury in cardiomyocytes and its cardioprotective effects in the pathogenesis of diabetic cardiomyopathy (DCM). H9C2 cells were treated with TNF-α with or without vaspin in vitro.

Autophagy attenuates endothelial-to-mesenchymal transition by promoting Snail degradation in human cardiac microvascular endothelial cells.

Endothelial-to-mesenchymal transition (EndMT) mainly exists in cardiovascular development and disease progression, and is well known to contribute to cardiac fibrosis. Recent studies indicated that autophagy also participates in the regulation of cardiac fibrosis. However, the precise role of autophagy in cardiac fibrosis and the underlying molecular mechanism remain unclear.

Predictive value of exercise-induced atrial natriuretic peptide secretion for the presence of left atrial low-voltage areas in patients with persistent atrial fibrillation.

Objectives Left atrial (LA) low-voltage areas (LVAs) are a strong predictor of atrial fibrillation (AF) recurrence after pulmonary vein isolation (PVI). However, a non-invasive method for evaluating LA-LAVs has not been established yet. The objective of our study was to assess the predictive value of the plasma atrial natriuretic peptide (ANP) level for the presence of LA-LVAs in patients with persistent AF (PeAF).

RUNX3 modulates hypoxia-induced endothelial-to-mesenchymal transition of human cardiac microvascular endothelial cells.

Endothelial-mesenchymal transition (EndMT) is an essential mechanism in the cardiovascular system, for both cardiovascular development and cardiovascular diseases (CVDs). Recent studies indicate that runt-related transcription factor 3 (RUNX3) contributes to EndMT and endothelial cell dysfunction. However, the underlying molecular mechanism remains unknown.

Fibrillatory wave amplitude on transesophageal ECG as a marker of left atrial low-voltage areas in patients with persistent atrial fibrillation.

Background: Low-voltage areas (LVAs) are frequently observed in patients with persistent atrial fibrillation (PeAF) and may represent adverse atrial remodeling. However, noninvasive method of evaluating LAVs is not well established.

Methods: In a cohort of 68 patients with PeAF, endocardial voltage maps of left atrium (LA) were created during sinus rhythm after pulmonary vein isolation (PVI).

[Knockdown of RUNX3 inhibits hypoxia-induced endothelial-to-mesenchymal transition of human cardiac microvascular endothelial cells].

Objective To investigate the effects of Runt-related transcription factor 3 (RUNX3) knockdown on hypoxia-induced endothelial-to-mesenchymal transition (EndoMT) of human cardiac microvascular endothelial cells (HCMECs), and elucidate the underlying molecular mechanism. Methods HCMECs were cultured in hypoxic conditions and infected with RUNX3-RNAi lentivirus to knock-down the expression of RUNX3. Reverse transcription PCR was performed to detect the mRNA expressions of RUNX3 and EndoMT related genes such as CD31, vascular endothelial cadherin (VE-cadherin), α-smooth muscle actin (α-SMA) and fibroblast-specific protein-1 (FSP-1); Western blotting was used to determine the protein expressions of RUNX3, CD31, α-SMA and another molecules involved in EndoMT; and immunofluorescence cytochemistry was applied to observe the colocalization of CD31 and α-SMA.

Protective effects of Notch1 signaling activation against high glucose-induced myocardial cell injury: Analysis of its mechanisms of action.

Notch1 plays an important role in cardiomyocyte apoptosis and cardiac fibrosis. However, the effects of Notch1 on diabetic cardiomyopathy (DCM) and its mechanisms of action remain unclear. In the present study, we sought to investigate the role of Notch1 in, and its effects on high glucose (HG)‑induced myocardial cell apoptosis and myocardial fibrosis.

[Research progress of Tbx3 in cardiac biological pacemaker].

The early cardiac biological pacemaker studies were mostly around HCN channel, and how to build a biological pacemaker through the enhanced If current. In recent years, however, people found that the genes of Tbx3 could play an important role in the development of cardiac conduction system, especially in processes of the maturity of the sinoatrial node and maintenance of its function. And the Tbx3 can further optimize the biological pacemaker.

Effect of NRG-1/ErbB signaling intervention on the differentiation of bone marrow stromal cells into sinus node-like cells.

The neuregulin-1 (NRG-1)/ErbB signaling pathway is a crucial regulator of cardiac development and plays an important role in the formation of the cardiac special conduction system. To establish a rat bone marrow stromal cell (BMSC) cardiomyocyte (CM)-like differentiation model, BMSCs were treated with 5-azacytidine and fibroblast growth factor basic (FGF-basic) for 24 hours and then cocultured with neonatal rat CMs in a Transwell culture system. The feasibility of regulating the differentiation of BMSCs into sinoatrial node cells by manipulating the NRG-1/ErbB pathway was investigated.

Gene transfer of human neuregulin-1 attenuates ventricular remodeling in diabetic cardiomyopathy rats.

Neuregulin-1 (NRG-1) is a cardioactive growth factor released from endothelial cells. However, the effect of NRG-1 on ventricular remodeling in diabetic cardiomyopathy (DCM) remains unclear. The aim of the present study was to investigate the pathophysiological role of NRG-1 in a rat model of DCM.

[Adipose tissue-derived adult stem cells transfected with the gene of hyperpolarization-activated cyclic nucleotide-gated ion channel 2 differentiated into pacemaker-like cells].

Objective: To transfect rat adipose tissue-derived adult stem cells (ADSCs) with the pacemaker gene of human hyperpolarization-activated cyclic nucleotide-gated ion channel 2 (hHCN2), and observe its feasibility of functioning as pacemaker cells.

Methods: First of all, healthy ADSCs were harvested and transfected with hHCN2 gene. Thereafter, we detected the expression of hHCN2 gene and protein by quantitative real-time PCR (qRT-PCR), Western blot analysis and immunofluorescence cytochemistry and measured the electrophysiological properties and recorded the inward currents using patch clamp techniques.

Therapeutic effects of neuregulin-1 gene transduction in rats with myocardial infarction.

Aim: In this study, we investigated whether lentivirus-mediated gene transduction improves the cardiac function in rats with myocardial infarction and the mechanisms involved.

Methods And Results: Briefly, lentivirus carrying human neuregulin-1 (hNRG-1) gene was injected into infarcted myocardium of rats. Four weeks later, lentivirus-mediated gene transduction promoted hNRG-1 gene and protein expression.

Therapeutic effects of neuregulin-1 in diabetic cardiomyopathy rats.

Background: Diabetic cardiomyopathy (DCM) is a disorder of the heart muscle in people with diabetes, which is characterized by both systolic and diastolic dysfunction. The effective treatment strategy for DCM has not been developed.

Methods: Rats were divided into 3 groups with different treatment.

Adipose tissue stromal cells transplantation in rats of acute myocardial infarction.

Objective: This study was to investigate the proliferation and differentiation of rat adipose stromal cells when implanted into ischemic myocardium and the improvement of heart function.

Methods: Sprague-Dawley rat adipose tissue was digested with collagenase type I solution and adipose stromal cells were derived by culture. The cells' surface phenotype was examined by flow cytometry.

Effect of cytokines secreted by human adipose stromal cells on endothelial cells.

To isolate and culture adipose stromal cells (ASCs), and study the effect of cytokines secreted by ASCs on endothelial cells, human adipose tissue was digested with collagenase type I solution and ASCs were derived by culture. The cells surface phenotype was examined by flow cytometry. ELISA was used to detect the secretion of VEGF, HGF, SDF-1 alpha and RT-PCR was employed to detect the expression of their mRNA.